R. Krapf et al., NEUTRAL PHOSPHATE ADMINISTRATION GENERATES AND MAINTAINS RENAL METABOLIC ALKALOSIS AND HYPERPARATHYROIDISM, American journal of physiology. Renal, fluid and electrolyte physiology, 37(5), 1995, pp. 802-807
We examined the effects of chronic intravenous neutral phosphate admin
istration on systemic acid-base equilibrium and parathyroid function i
n six normal, NaCl-replete male human subjects under metabolic balance
conditions. The subjects received 4.35 mmol of neutral sodium phospha
te . kg body wt(-1) . day(-1) intravenously and continuously for 7 day
s and the same amount of sodium as NaCl during control and recovery. B
lood pH increased from 7.388 to 7.411 (P < 0.001) and plasma bicarbona
te from 23.5 to 26.0 mmol/l (P < 0.001). Urinary pH increased from 6.5
8 to 6.79 (P < 0.001). Net acid excretion increased from 59 to 100 mmo
l/24 h (P < 0.001). Plasma ionized calcium concentration decreased and
plasma phosphate concentration increased transiently. Serum intact pa
rathyroid hormone increased from 24 to 62 pg/ml (P < 0.001). Chronic p
hosphate administration also resulted in a significant increase in ren
al phosphate clearance (35 to 229 ml/min) and decrease in the fraction
al excretion of calcium (1.8 to 0.9%). Thus chronic intravenous phosph
ate administration generates and maintains renal metabolic alkalosis i
n salt-replete humans and induces hyperparathyroidism. The severity of
metabolic alkalosis is mitigated by an apparent increase in effective
endogenous acid production as evidenced by the significant increase i
n steady-state net acid excretion.